In a state of oxidative stress, there is an increase of reactive species, which induce an altered intracellular signaling, leading to dysregulation of the inflammatory response. The inability of the antioxidant defense systems to modulate the proinflammatory response is key to the onset and progression of neurodegenerative diseases. The aim of this work is to review the effect of the state of oxidative stress on the loss of regulation of the inflammatory response on the microglia and astrocytes, the induction of different CD4+T cell populations in neuroinflammation, as well as its role in some neurodegenerative diseases. For this purpose, an intentional search of original articles, short communications, and reviews, was carried out in the following databases: PubMed, Scopus, and Google Scholar. The articles reviewed included the period from 1997 to 2017. With the evidence obtained, we conclude that the loss of redox balance induces alterations in the differentiation and number of CD4+T cell subpopulations, leading to an increase in Th1 and Th17 response. This contributes to the development of neuroinflammation as well as loss of the regulation of the inflammatory response in neurodegenerative diseases such as Alzheimer's (AD), Parkinson's (PD), and Multiple Sclerosis (MS). In contrast, regulatory T cells (Tregs) and Th2 modulate the inflammatory response of effect of T cells, microglia, and astrocytes. In this respect, it has been found that the mobilization of T cells with anti-inflammatory characteristics toward damaged regions of the CNS can provide neuroprotection and become a therapeutic strategy to control inflammatory processes in neurodegeneration.

Our data suggest that the cytokine balance is broken, encouraging the development of an exacerbated inflammatory response. Our results show that there is a shift, in the Th1/Th2, and the Th17/Treg balance, favoring skewness towards a proinflammatory status in the umbilical cord blood in preeclampsia.

No abstract

In breast cancer, an uncontrolled cell proliferation leads to tumor formation and development of a multifactorial disease. Metastasis is a complex process that involves tumor spread to distant parts of the body from its original site. Metastatic dissemination represents the main physiopathology of cancer. Inter-and intracellular communication in all systems in vertebrates is mediated by cytokines, which are highly inducible, secretory proteins, produced not only by immune system cells, but also by endocrine and nervous system cells. It has become clear in recent years that cytokines, as well as their receptors are produced in the organisms under physiological and pathological conditions; recently, they have been closely related to breast cancer metastasis. The exact initiation process of breast cancer metastasis is unknown, although several hypotheses have emerged. In this study, we thoroughly reviewed the role of several cytokines in breast cancer metastasis. Data reviewed suggest that cytokines and growth factors are key players in the breast cancer metastasis induction. This knowledge must be considered with the aim to development of new therapeutic approaches to counter breast cancer metastasis.

No abstract

Introduction 3. Behavioral effects caused by BPA 3.1. Memory and learning disorders 3.2. Anxiety and depressive-like behaviors 3.3. Socio-sexual behavior 4. BPA and neurodegenerative disorders 4.1. Parkinson's disease and BPA exposure 4.2. Amyotrophic lateral sclerosis and BPA 4.3. Multiple sclerosis and BPA 5. BPA and neurodevelopmental disorders 5.1. Autism spectrum disorders and BPA 5.2. Attention-deficit/hyperactivity disorder and BPA 6. Potential mechanisms behind BPA and neurological disorders 6.1. Endocrine-related mechanisms 6.2. Epigenetic mechanisms 6.3. Mitochondrial pathways 6.4. Calcium and oxidative stress pathways 6.5. Inflammatory response pathways 7. Conclusions 8. Acknowledgments 9. References Effects of BPA on behavior, neurodevelopment and neurodegenerative disorders 364 © 1996-2021 function, behavioral disturbances, neurodegenerative diseases (Parkinson´s Disease, Amyotrophic lateral sclerosis, Multiple Sclerosis), and neurodevelopmental disorders (Autism Spectrum and Attention-Deficit/Hyperactivity Disorders). Likewise, the molecular and cellular mechanisms that may be involved with these pathological conditions will be analyzed.

SARS-CoV-2 causes COVID-19, which has claimed millions of lives. This virus can infect various cells and tissues, including the brain, for which numerous neurological symptoms have been reported, ranging from mild and nonlife-threatening (e.g., headaches, anosmia, dysgeusia, and disorientation) to severe and life-threatening symptoms (e.g., meningitis, ischemic stroke, and cerebral thrombosis). The cellular receptor for SARS-CoV-2 is angiotensinconverting enzyme 2 (ACE2), an enzyme that belongs to the renin-angiotensin system (RAS). RAS is an endocrine system that has been classically associated with regulating blood pressure and fluid and electrolyte balance; however, it is also involved in promoting inflammation, proliferation, fibrogenesis, and lipogenesis. Two pathways constitute the RAS with counter-balancing effects, which is the key to its regulation. The first axis (classical) is composed of angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and angiotensin type 1 receptor (AT1R) as the main effector, which -when activated-increases the production of aldosterone and antidiuretic hormone, sympathetic nervous system tone, blood pressure, vasoconstriction, fibrosis, inflammation, and reactive oxygen species (ROS) production. Both systemic and local classical RAS' within the brain are associated with cognitive impairment, cell death, and inflammation. The second axis (non-classical or alternative) includes ACE2, which converts Ang II to Ang-(1-7), a peptide molecule that activates Mas receptor (MasR) in charge of opposing Ang II/AT1R actions. Thus, the alternative RAS axis enhances cognition, synaptic remodeling, cell survival, cell signal transmission, and antioxidant/anti-inflammatory mechanisms in the brain. In a physiological state, both RAS axes remain balanced. However, some Frontiers in Cellular Neuroscience 01 frontiersin.org Méndez-García et al. 10.3389/fncel.2022.977039factors can dysregulate systemic and local RAS arms. The binding of SARS-CoV-2 to ACE2 causes the internalization and degradation of this enzyme, reducing its activity, and disrupting the balance of systemic and local RAS, which partially explain the appearance of some of the neurological symptoms associated with COVID-19. Therefore, this review aims to analyze the role of RAS in the development of the neurological effects due to SARS-CoV-2 infection. Moreover, we will discuss the RAS-molecular targets that could be used for therapeutic purposes to treat the short and long-term neurological COVID-19-related sequelae.

TRIM25 is emerging as a central factor in breast cancer due to its regulation and function. In particular, it has been shown that: (1) Estrogens modulate TRIM25 gene expression; (2) TRIM25 has activity as an E3-ligase enzyme for ubiquitin; and (3) TRIM25 is also an E3 ligase for interferon-stimulated gene 15 protein in the ISGylation system. Consequently, the proteome of mammary tissue is affected by TRIM25-associated pathways, involved in tumor development and metastasis. Here, we discuss the findings on the mechanisms involved in regulating TRIM25 expression and its functional relevance in breast cancer progression. These studies suggest that TRIM25 may be a biomarker and a therapeutic target for breast cancer.